Thromb Haemost 2002; 88(02): 335-344
DOI: 10.1055/s-0037-1613207
In Focus
Schattauer GmbH

Quenching of Intracellular ROS Generation as a Mechanism for Oleate-Induced Reduction of Endothelial Activation and Early Atherogenesis

Marika Massaro
1   Laboratory for Thrombosis and Vascular Research, C.N.R. Institute of Clinical Physiology, Pisa
3   Department of Experimental Pathology, the University of Pisa
,
Giuseppina Basta
1   Laboratory for Thrombosis and Vascular Research, C.N.R. Institute of Clinical Physiology, Pisa
,
Guido Lazzerini
1   Laboratory for Thrombosis and Vascular Research, C.N.R. Institute of Clinical Physiology, Pisa
,
Maria Annunziata Carluccio
2   Lecce, University of Pisa
,
Francesca Bosetti
4   Biochemistry Section, Scuola Superiore S. Anna, Pisa
,
Giancarlo Solaini
4   Biochemistry Section, Scuola Superiore S. Anna, Pisa
,
Francesco Visioli
5   Institute of Pharmacological Sciences, University of Milan
,
Aldo Paolicchi
3   Department of Experimental Pathology, the University of Pisa
,
Raffaele De Caterina
1   Laboratory for Thrombosis and Vascular Research, C.N.R. Institute of Clinical Physiology, Pisa
6   Chair of Cardiology, “G. d’Annunzio” University, Chieti, Italy
› Author Affiliations
Further Information

Publication History

Received 30 November 2001

Accepted after revision 30 April 2002

Publication Date:
07 December 2017 (online)

Summary

We previously showed that the exposure of vascular endothelium to oleate results in reduced endothelial activation. We now investigate possible mechanisms for this effect in relation to generation of reactive oxygen species (ROS). We stimulated several types of endothelial cells with cytokines or lipopolysaccharide, with or without preincubation with 10-100 µmol/L oleate. Oleate preincubation reduced VCAM-1 expression in all cell types, as well as macrophage-colony stimulating factor release. We simultaneously measured the concentration of intracellular glutathione (GSH), the activity of GSH-related antioxidant enzymes and the production of intracellular ROS. Stimulation of endothelial cells caused a decrease of GSH and an increase in intracellular ROS. The addition of oleate before stimulation, prevented the depletion of GSH and partially prevented stimuli-induced increase of intracellular ROS. This occurred without any change in the activity of GSH-related antioxidant enzymes, superoxide dismutase and catalase. Furthermore, in a cell-free superoxide anion-generating system, oleate quenched the generation of ROS. These results indicate that oleate may exert direct vascular atheroprotective effects by inhibiting endothelial activation through a quenching of stimuli-induced increase in ROS.

 
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